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Biomedical subjects

H Yaku

Publications and source records attributed to H Yaku.

At least 37 records · Page 2Linked to original sources
PubMed1997

Dynamic cardiac compression improves contractile efficiency of the heart.

The effect of dynamic cardiac compression on left ventricular contractile efficiency was assessed in terms of the pressure-volume relationship and myocardial oxygen consumption. In 11 excised cross-circulated dog hearts, the ventricle was directly compressed during systole (dynamic cardiac compression). Measurements for pressure-volume area (a measure of total mechanical energy), external work, and myocardial oxygen consumption were done before and during dynamic cardiac compression. Dynamic cardiac compression increased pressure-volume area by 28% +/- 17% (mean plus or minus the standard deviation) and external work by 24% +/- 20% (p = 0.0000185 and 0.0000212, respectively) at given end-diastolic and stroke volumes without affecting myocardial oxygen consumption. As a result, the oxygen cost of pressure-volume area, that is, the slope of the myocardial oxygen consumption-pressure-volume area relationship, significantly decreased by 16% +/- 13% (p = 0.0000135) whereas the pressure-volume area-independent myocardial oxygen consumption was unchanged. Then, contractile efficiency, that is, the reciprocal of the slope of the myocardial oxygen consumption-pressure-volume area relationship in joules significantly improved from 45% +/- 8% to 53% +/- 13% (p = 0.0000437). When the native myocardial oxygen consumption-pressure-volume area relationship was assessed by subtracting the dynamic cardiac compression pressure applied to the heart, the slope of the myocardial oxygen comsumption-pressure-volume area relationship returned to the control level. This indicates that the contractile efficiency of the native heart was not affected by dynamic cardiac compression. We conclude that dynamic cardiac compression enhances left ventricular pump function by improving the contractile efficiency of the overall heart leaving the energetics of the native heart unchanged.

Animals↗
PubMed1997

Intraatrial rerouting in left isomerism and late complications.

We performed a total repair for a 1-year-old boy with left isomerism, a common atrium, incomplete atrioventricular septal defect and hemiazygos continuation. The operation performed was intraatrial rerouting with a baffle and mitral repair. The postoperative course was uneventful. However, two and a half years after the total repair, the patient revealed obstruction of the systemic atrium constructed by the baffle and the left ventricular outflow tract. Reoperation to relieve these obstructions was successful.

Cardiac Surgical Procedures↗
PubMed1996

Dissection of the ascending aorta: a late complication of coronary artery bypass grafting.

Acute dissection of the ascending aorta as a late complication of coronary artery bypass grafting has been rarely reported. We report a case of a 61 year-old man in whom acute dissection of the ascending aorta developed 2 years after coronary artery bypass grafting. The ascending aorta was replaced with a Dacron graft, and an island of the aortic wall, on which previous proximal anastomoses had been placed, was implanted into the Dacron graft successfully.

Acute Disease↗
PubMed1995

Successful repair of a ruptured postinfarct pseudoaneurysm of the left ventricle.

We report a case of a 60-year-old woman who underwent emergency surgical repair of a ruptured pseudoaneurysm of the left ventricle 10 days after acute myocardial infarction. The repair consisted of oversewing the rupture (2 cm long) on the posterior wall under cardiopulmonary bypass. The patient made a satisfactory recovery.

Aneurysm, False↗
PubMed1994

The Dbl oncogene product as a GDP/GTP exchange protein for the Rho family: its properties in comparison with those of Smg GDS.

The dbl oncogene product (Dbl) showed the GDP/GTP exchange protein (GEP) activity on all the rho family small GTP-binding protein (G protein) members including RhoA and Rac1 as well as mCdc42. Dbl was active on both the lipid-modified and -unmodified forms of these small G proteins, but was much more active on the former form than on the latter form. In the presence of Rho GDI, an inhibitory GEP for the rho family members, the GEP activity of Dbl was markedly reduced. These properties of Dbl were partly different from those of Smg GDS, another GEP which is active not only on the rho family members but also on Ki-Ras and Rap1 and is active only on their lipid-modified form.

GTP-Binding Proteins↗
PubMed1994

Improvement of gas exchange following endobronchial instillation of an exogenous surfactant in an infant with respiratory failure by postoperative pulmonary haemorrhage.

We administered surfactant to a 5-month-old infant with respiratory failure due to right pulmonary haemorrhage accompanied by oedema following abdominal surgery. These pathological conditions were probably precipitated by disseminated intravascular coagulation and intra-operative excessive administration of fluids, respectively. Endobronchial instillation of the exogenous surfactant (120 mg) after selective intubation of the right bronchus produced a dramatic improvement of gas exchange 30 min after treatment and of chest X-ray findings at 6 h post-treatment. This case on an infant indicates that administration of surfactant may be one of promising therapeutic approaches to respiratory failure due to pulmonary haemorrhage.

Biliary Atresia↗
PubMed1994

Effect of lidocaine pretreatment on endotoxin-induced lung injury in rabbits.

BACKGROUND: It is well known that endotoxin causes acute lung injury resulting in adult respiratory distress syndrome. Numerous cellular and humoral factors such as macrophages, neutrophils, platelets, and inflammatory mediators (e.g., activated complements, cytokines, and arachidonic acid metabolites) are thought to play a pivotal role in the pathogenesis of endotoxin-induced lung injury. Furthermore, pulmonary edema in acute lung injury is associated with an increase in vascular permeability that may arise from a perturbation of the endothelial cell surface membrane. Lidocaine has been shown to inhibit function of these cells and stabilize cell membranes. The aim of the current study was to determine whether pretreatment with intravenous lidocaine could attenuate acute lung injury induced by endotoxin in rabbits. METHODS: Twenty-seven anesthetized male rabbits were randomly assigned to receive one of three treatments (n = 9 for each group); infusion of saline (as a control), infusion of Escherichia coli endotoxin (30 micrograms kg-1 over a 60-min period) without treatment with lidocaine, and infusion of endotoxin with treatment with lidocaine. A single dose of intravenous lidocaine 2 mg.kg-1 was administered 10 min before infusion of endotoxin and thereafter infused at a rate of 2 mg.kg-1.h-1 until 6 h after the start of endotoxin administration, when the animals were killed. The lungs of the rabbits were ventilated with 40% oxygen. Hemodynamics, peripheral leukocytes counts, and arterial oxygen tension were recorded during the ventilation period. After the observation, lung mechanics, cell fraction of bronchoalveolar lavage fluid (BALF), activated complements, cytokines, and arachidonic acid metabolites concentrations in BALF were measured and analyzed. The lung wet-to-dry-weight ratio and albumin concentrations in BALF were analyzed as an indices of pulmonary edema. The cypridina luciferin analog-dependent chemiluminescence (representing superoxide production) by neutrophils isolated from the pulmonary artery and light microscopic findings were compared among the three groups. RESULTS: Endotoxin caused decreases in peripheral leukocyte counts, lung compliance, and arterial oxygen tension, and increases in the lung wet-to dry-weight ratio, polymorphonuclear cell counts in BALF, and albumin, C3a, C5a, tumor necrosis factor alpha, interleukin-1 beta, and thromboxane B2 concentrations in BALF. Lidocaine pretreatment attenuated these changes. The cypridina luciferin analog--dependent chemiluminescence was greater in rabbits receiving endotoxin than in the control. Lidocaine pretreatment attenuated the increase in chemiluminescence. Endotoxin caused extensive morphologic lung damage, which was lessened by lidocaine. CONCLUSIONS: These results suggest that intravenous lidocaine pretreatment has a prophylactic effect on endotoxin-induced lung injury in rabbits. However, further studies are required to investigate the therapeutic (as an early posttreatment) effect of the drug given after lung injury because rabbits in the current study received lidocaine before endotoxemia.

Animals↗
PubMed1994

Partial attenuation of the cardiovascular responses to tracheal intubation with oral manidipine.

We conducted a placebo-controlled, randomized, and double-blinded study to evaluate the efficacy of manidipine given orally in attenuating the cardiovascular responses to laryngoscopy and tracheal intubation. Thirty normotensive patients (ASA physical status 1) undergoing elective surgery were allocated to one of three groups (n = 10 for each); placebo, 5 mg manidipine, and 10 mg manidipine groups. These tablets were orally administered 3 h before induction of anaesthesia. Anaesthesia was induced with thiopentone 5 mg.kg-1 iv, and tracheal intubation was facilitated with vecuronium 0.2 mg.kg-1. Laryngoscopy lasting 30 sec was attempted 2 min after induction of anaesthesia. Patients receiving placebo showed a significant increase in systolic and diastolic blood pressure associated with tracheal intubation. These increases following tracheal intubation were significantly reduced in patients receiving manidipine 10 mg compared with patients receiving placebo or manidipine 5 mg (P < 0.05). Oral administration of manidipine 10 mg before induction of anaesthesia is a simple and effective method for attenuating pressor response to laryngoscopy and tracheal intubation. We stressed that the potential beneficial effect of a reduced haemodynamic reaction to intubation might be obtained at the expense of hypotension later on.

Administration, Oral↗
PubMed1994

rac p21 is involved in insulin-induced membrane ruffling and rho p21 is involved in hepatocyte growth factor- and 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced membrane ruffling in KB cells.

Insulin and hepatocyte growth factor (HGF) induced morphologically different membrane rufflings in KB cells. Insulin-induced membrane ruffling was inhibited by microinjection of rho GDI, an inhibitory GDP/GTP exchange regulator for both rho p21 and rac p21 small GTP-binding proteins, but not inhibited by microinjection of botulinum exoenzyme C3, known to selectively ADP-ribosylate rho p21 and to impair its function. This rho GDI action was prevented by comicroinjection with guanosine 5'-(3-O-thio)triphosphate (GTP gamma S)-bound rac1 p21. In contrast, HGF-induced membrane ruffling was inhibited by microinjection of rho GDI or C3. This rho GDI action was prevented by comicroinjection with GTP gamma S-bound rhoA p21, and this C3 action was prevented by comicroinjection with GTP gamma S-bound rhoAIle-41 p21, which is resistant to C3. Microinjection of either GTP gamma S-bound rac1 p21 or rhoA p21 alone induced membrane ruffling in the absence of the growth factors. The rac1 p21-induced membrane ruffling was morphologically similar to the insulin-induced kind, whereas rhoA p21-induced ruffling was apparently different from both the insulin- and HGF-induced kinds. Membrane ruffling was also induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), a protein kinase C-activating phorbol ester, but not by Ca2+ ionophore or microinjection of a dominant active Ki-ras p21 mutant (Ki-rasVal-12 p21). The phorbol ester-induced membrane ruffling was morphologically similar to the rhoA p21-induced kind and inhibited by microinjection of rho GDI or C3. These results indicate that rac p21 and rho GDI are involved in insulin-induced membrane ruffling and that rho p21 and rho GDI are involved in HGF- and phorbol ester-induced membrane rufflings.

ADP Ribose Transferases↗
PubMed1994

Effects of free wall ischemia and bundle branch block on systolic ventricular interaction in dog hearts.

Systolic direct ventricular interaction is thought to occur via the ventricular septum and the coordinated contraction of common fibers shared by both ventricles. The purpose of the present study was to evaluate the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary artery occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interaction, we used an abrupt hemodynamic perturbation (aortic constriction), and we measured systolic interaction gain (IG) as delta right ventricular peak systolic pressure/delta left ventricular peak systolic pressure (IG(peak)) and instantaneous delta right ventricular pressure/delta left ventricular pressure at matched data sampling times (IG(inst)), along with changes in right ventricular stroke volume and stroke work before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmission contribution to ventricular interaction, the delta left ventricular peak systolic pressure produced by the aortic constriction was matched under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0.11 +/- 0.05. These values did not change with either free wall ischemia or ventricular pacing, with or without an intact pericardium. The changes in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either ischemia or ventricular pacing, with or without an intact pericardium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

The effects of dynamic cardiac compression on ventricular mechanics and energetics. Role of ventricular size and contractility.

The purpose of this study was to determine the role of ventricular size or contractility in the effectiveness of dynamic cardiac compression in terms of the pressure-volume relationship and myocardial oxygen consumption. In 10 isolated cross-circulated dog hearts, the ventricle was directly compressed during systole. For the volume run, measurements for slope of the end-systolic pressure-volume relation, pressure-volume area, external work, coronary blood flow, and myocardial oxygen consumption were achieved before and during a fixed amount of dynamic cardiac compression. Left ventricular volume was then increased while stroke volume was kept constant, and measurements were repeated. For the contractility run, after the control measurements were taken, left ventricular contractility was significantly increased or decreased by infusion of either dobutamine or propranolol into the coronary circulation. Measurements were repeated before and during dynamic cardiac compression at the control level of end-diastolic and stroke volumes. Dynamic cardiac compression significantly increased slope of the end-systolic pressure-volume relation, pressure-volume area, and external work (p < 0.01), whereas coronary blood flow and myocardial oxygen consumption were not affected. The increase in pressure-volume area caused by dynamic cardiac compression was greater with the larger volume. Despite the significant differences in the native left ventricular contractility, the increases in slope of the end-systolic pressure-volume relation, pressure-volume area, and external work did not differ among the three groups. We conclude that dynamic cardiac compression enhances left ventricular systolic function independent of ventricular contractility and without affecting coronary blood flow or myocardial oxygen consumption. Mechanical enhancement is more effective in the dilated heart.

Animals↗
PubMed1993

Regulation of morphology by rho p21 and its inhibitory GDP/GTP exchange protein (rho GDI) in Swiss 3T3 cells.

rho GDP dissociation inhibitor (GDI) is an inhibitory GDP/GTP exchange protein for a group of small GTP-binding proteins including at least rhoA p21, rhoB p21, rac1 p21, rac2 p21, and G25K. Microinjection of rho GDI into Swiss 3T3 cells made the cells round and refractile. This morphological change was accompanied by the disappearance of stress fibers. The rho GDI action was prevented by comicroinjection of rho GDI with the guanosine 5'-(3-O-thio)triphosphate (GTP gamma S)-bound form of rhoA p21, but not with the GTP gamma S-bound form of rhoA p21 lacking the C-terminal three amino acids, which was not post-translationally modified with lipids. The GTP gamma S-bound form of rac1 p21, the same form of G25K, the same form of smg p21B, or Ki-rasval12 p21 was ineffective. Microinjection of the bacterial ADP-ribosyltransferase C3 specific for rho p21 into Swiss 3T3 cells induced the similar changes of morphology and stress fibers. This C3 action was not prevented by comicroinjection of C3 with the GTP gamma S-bound form of rhoA p21, but was prevented by comicroinjection with the same form of a rhoA p21 mutant which was not ADP-ribosylated by C3. These results indicate that the rho GDI-rho p21 system regulates cell morphology presumably through the actomyosin system in Swiss 3T3 cells.

3T3 Cells↗
PubMed1993

Perioperative changes in superoxide production in neonates and infants.

We conducted a prospective study to investigate perioperative changes in the production of superoxide anion (O2-) by neutrophils isolated from ten neonates between the ages of five and 16 days (N group) and ten infants ranging in age from one to ten months (I group). They underwent abdominal surgery under general anaesthesia with halothane and nitrous oxide in oxygen. The O2- production (speed and amount) was measured perioperatively using the cytochrome c reduction method. Both groups showed a decrease in the speed and amount of O2- production during and after surgery. The decrease in O2- production reached its lowest level three hours postoperatively or at the end of surgery in both groups. The O2- production in the I group returned to the basal value 48 hr postoperatively. In contrast, the O2- production in the N group was still lower 48 hr after surgery than before anaesthesia. Although the total amount of O2- production by neutrophils in one mL of peripheral blood remained unchanged in the I group, the total amount of O2- production in the N group decreased at the end of surgery and thereafter. These data indicate that even relatively minor abdominal surgery with halothane anaesthesia may be associated with perioperative neutrophil impairment in both neonates and infants. This impairment of neutrophil function in infants but not in neonates may be compensated by an increase in neutrophil numbers. It is possible that perioperative susceptibility of neonates to bacterial infections is attributable, at least in part, to the inhibition of O2- production in neutrophils by surgery and general anaesthesia.

Abdomen↗
PubMed1993

Efficacy of oral clonidine premedication in children.

BACKGROUND: Clonidine, an alpha 2-adrenoceptor agonist, has been shown to be effective as a preanesthetic medication in adults. The current study was designed to investigate the efficacy of two doses of oral clonidine as a premedicant preceding oral atropine in children. METHODS: In a prospective, randomized, double-blind, controlled clinical trial, 105 children, aged 4-12 yr, undergoing elective ophthalmologic surgery received 0.4 mg/kg diazepam, 2 micrograms/kg clonidine, or 4 micrograms/kg clonidine orally. These agents mixed with apple juice were administered 105 min before the estimated time of induction of anesthesia, and were followed by treatment with 0.03 mg/kg oral atropine 60 min before anesthesia. A blinded observer noted the children's level of sedation, quality of separation from parents, and degree of acceptance of mask application during inhalation of nitrous oxide used for establishment of venous access. Anesthesia was induced with 5 mg/kg thiamylal, and tracheal intubation was facilitated with 0.2 mg/kg vecuronium. Hemodynamic changes after tracheal intubation were compared among the three groups. RESULTS: Clonidine produced significant sedation, and the effect was dose related. Clonidine, 4 micrograms/kg, provided better quality of separation and acceptance of mask than the two other regimens. This dose of clonidine attenuated the increases in blood pressure and heart rate after tracheal intubation. No clinically significant perioperative hypotension or bradycardia was observed. CONCLUSIONS: These data indicate that, even in pediatric surgery, the combination of 4 micrograms/kg and 0.03 mg/kg oral clonidine is an effective premedication. However, the safety and optimal dose of clonidine in this setting remain to be determined.

Administration, Oral↗
PubMed1993

Attenuation of the pressor response to tracheal intubation with oral nitrendipine.

The effect of nitrendipine on the cardiovascular responses to tracheal intubation was studied in a placebo-controlled, randomised, double-blind trial. Thirty patients (ASA physical status 1) undergoing elective surgery received either 5 or 10 mg nitrendipine, or a placebo orally 3 h before induction of anaesthesia (n = 10 for each group). Anaesthesia was induced with sodium thiopentone 5 mg/kg i.v. and tracheal intubation was facilitated with vecuronium 0.2 mg/kg i.v. Patients receiving the placebo showed a significant increase in the mean arterial pressure and the rate-pressure product in response to tracheal intubation. These increases following intubation were reduced in nitrendipine-treated patients compared with the placebo group (P < 0.05). Oral administration of nitrendipine (5 or 10 mg, 3 h before induction of anaesthesia) was able to attenuate the hypertensive response to tracheal intubation in ASA 1 patients under light anaesthesia. We propose this pharmacological technique with supplementary doses of opioids and/or benzodiazepines for the management of patients with hypertension or coronary artery disease.

Administration, Oral↗
PubMed1993

Effects of 2-, 4- and 12-hour fasting intervals on preoperative gastric fluid pH and volume, and plasma glucose and lipid homeostasis in children.

We evaluated 105 randomly-selected unpremedicated children aged 1-14 years to determine the effects of a 2-, 4- and 12-h preoperative fasting interval on the preoperative gastric fluid pH and volume, and plasma glucose and lipid homeostasis. Each child undergoing elective surgery ingested a large volume (approximately 10 ml/kg b.w.) of apple juice and then fasted for 2, 4 or 12 h before the estimated induction of anaesthesia. After induction of anaesthesia, gastric fluid was aspirated through a large-bore, multiorifice orogastric tube. Plasma concentrations of glucose, total ketone bodies, non-esterified fatty acid (NEFA), triglycerides, and cortisol were measured at the time of induction to evaluate the fasting interval effects on preoperative plasma glucose and lipid homeostasis. There were no significant differences between the three groups in either gastric fluid volume or pH. In addition, there were no significant differences between the groups with respect to the proportion with a pH < 2.5 and volume > 0.4 ml/kg b.w. Neither plasma concentrations of glucose, triglycerides, nor cortisol at the time of anaesthetic induction differed between the three groups. Both 4 and 12 h nil per os (NPO) caused an increase in lipolysis, which was presumably a compensatory mechanism to maintain normoglycaemia. The plasma NEFA and total ketone bodies concentrations were therefore significantly higher in these two fasting intervals than in 2 h NPO. These data suggest that a 2-h NPO, after a large volume of ingested apple juice, may offer additional benefits by preventing an increase in lipolysis during the fasting interval without either increasing the volume of gastric fluid or decreasing the gastric pH.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗